Zusammenfassung
In der Genese der essentiellen Hypertonie wird einer erhöhten Kochsalzzufuhr zwar nicht ausschließliche, dennoch aber große Bedeutung beigemessen [1]. Loew stellte bei nierengesunden Probanden einen NaCl-Verzehr von 13,1 ± 5,6 g/Tag fest [2], Schlierf hingegen durchschnittlich 11,32 g/Tag [3]. Während Kesteloot et al. (1980) darauf hinwiesen, daß sie bei zurückgehendem Na-Konsum in Belgien keine positive Korrelation mehr zwischen NaCl-Aufnahme und Blutdruck (BD) entgegen früheren Untersuchungen feststellen konnten [4], erschien im April 1982 von demselben Autor ein Artikel, der über eine positive Korrelation zwischen Gesamtserumkalzium und systolischem sowie diastolischem BD berichtete [5]. Kurze Zeit später veröffentlichte McCarron zwei Artikel, in denen er einerseits eine negative Korrelation zwischen ionisiertem Serumkalzium und dem BD von Normo- bzw. Hypertonikern mitteilte — das Gesamtserumkalzium war nicht mit dem BD korreliert [6]; andererseits wies er auf eine negative Korrelation zwischen diätetischer Kalziumzufuhr und Hypertonie hin [7]. Erste Hinweise auf die Verbindung erniedrigtes Kalzium — hoher systolischer BD lieferte Langford bereits 1973, als er über einen signifikant höheren Na/Ca-Quotienten im Urin bei einem systolischen BD > 125 mm Hg gegenüber < 105 mm Hg berichtete [8].
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Zimmermann, W. et al. (1984). Postersession V. In: 90. Kongreß. Verhandlungen der Deutschen Gesellschaft für Innere Medizin, vol 90. J.F. Bergmann-Verlag, Munich. https://doi.org/10.1007/978-3-642-85457-6_72
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